Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase, which is an essential
player in regulating cell migration, invasion, adhesion, proliferation, and survival. Its overexpression
and activation have been identified in sixty-eight percent of epithelial ovarian cancer patients and
this is significantly associated with higher tumor stage, metastasis, and shorter overall survival of
these patients. Most recently, a new role has emerged for FAK in promoting resistance to taxane and
platinum-based therapy in ovarian and other cancers. The development of resistance is a complex
network of molecular processes that make the identification of a targetable biomarker in platinum
and taxane-resistant ovarian cancer a major challenge. FAK overexpression upregulates ALDH and
XIAP activity in platinum-resistant and increases CD44, YB1, and MDR-1 activity in taxaneresistant
tumors. FAK is therefore now emerging as a prognostically significant candidate in this regard,
with mounting evidence from recent successes in preclinical and clinical trials using small
molecule FAK inhibitors. This review will summarize the significance and function of FAK in ovarian
cancer, and its emerging role in chemotherapeutic resistance. We will discuss the current status
of FAK inhibitors in ovarian cancers, their therapeutic competencies and limitations, and further
propose that the combination of FAK inhibitors with platinum and taxane-based therapies could be
an efficacious approach in chemotherapeutic resistant disease.
Programmed Death Ligand 1 (PD-L1) Expression in Epithelial Ovarian Cancer: A Comparison of Type I and Type II Tumors